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PubMed1989

Expression of cell adhesion molecule E-cadherin in Xenopus embryos begins at gastrulation and predominates in the ectoderm.

The expression of the Ca2+-dependent epithelial cell adhesion molecule E-cadherin (also known as uvomorulin and L-CAM) in the early stages of embryonic development of Xenopus laevis was examined. E-Cadherin was identified in the Xenopus A6 epithelial cell line by antibody cross-reactivity and several biochemical characteristics. Four independent mAbs were generated against purified Xenopus E-cadherin. All four mAbs recognized the same polypeptides in A6 cells, adult epithelial tissues, and embryos. These mAbs inhibited the formation of cell contacts between A6 cells and stained the basolateral plasma membranes of A6 cells, hepatocytes, and alveolar epithelial cells. The time of E-cadherin expression in early Xenopus embryos was determined by immunoblotting. Unlike its expression in early mouse embryos, E-cadherin was not present in the eggs or early blastula of Xenopus laevis. These findings indicate that a different Ca2+-dependent cell adhesion molecule, perhaps another member of the cadherin gene family, is responsible for the Ca2+-dependent adhesion between cleavage stage Xenopus blastomeres. Detectable accumulation of E-cadherin started just before gastrulation at stage 9 1/2 and increased rapidly up to the end of gastrulation at stage 15. In stage 15 embryos, specific immunofluorescence staining of E-cadherin was discernible only in ectoderm, but not in mesoderm and endoderm. The ectoderm at this stage consists of two cell layers. The outer cell layer of ectoderm was stained intensely, and staining was localized to the basolateral plasma membrane of these cells. Lower levels of staining were observed in the inner cell layer of ectoderm. The coincidence of E-cadherin expression with the process of gastrulation and its restriction to the ectoderm indicate that it may play a role in the morphogenetic movements of gastrulation and resulting segregation of embryonic germ layers.

Age Factors↗

PubMed1984

Ectodermal fragments from normal frog gastrulae condition substrata to support normal and hybrid mesodermal cell migration in vitro.

Using time-lapse cinemicrography and scanning electron microscopy, we have shown that normal Rana embryos and gastrulating hybrid embryos have extracellular fibrils on the inner surface of the ectodermal layer. These fibrils are absent prior to gastrulation and appear in increasing numbers during gastrulation. They can also be deposited in vitro where they condition substrata in such a way that normal presumptive mesodermal cells placed on them show extensive attachment and unoriented cell movement. These fibrils are also present in some arrested hybrid embryos, but in reduced numbers, or are lacking in other arrested hybrid embryos. Explanted ectodermal fragments from arrested hybrid embryos fail both to condition culture substrata by the deposition of fibrils and to promote cell attachment and translocation. In contrast, ectodermal fragments from normal embryos can condition culture substrata so as to promote moderate cell attachment and, for one particular gamete combination, even cell translocation of presumptive mesodermal cells taken from arrested hybrid embryos. These results provide new evidence to support the hypothesis that extracellular fibrils represent a system that promotes mesodermal cell migration in amphibian embryos. Differences in the fibrillar system in urodele and anuran embryos are discussed in relation to fundamental differences in the mode of mesodermal cell migration in these two classes of Amphibia.

Animals↗

PubMed2025

Noninvasive preimplantation genetic testing for aneuploidy using blastocyst spent culture medium may serve as a backup of trophectoderm biopsy in conventional preimplantation genetic testing.

BACKGROUND: To investigate whether the noninvasive preimplantation genetic testing (niPGT) complement conventional preimplantation genetic testing (PGT) in the embryos for aneuploidy. RESULTS: 40 spent culture medium (SCM) samples from routine embryo culture were collected, and half of each SCM (10 µL) sample was used for whole genome amplification, while the other half was stored at -80 °C for 3-6 months. Thirty-six out of 40 fresh SCM samples were successfully amplified and sequenced. Thirty-six paired frozen-thawed SCM samples showed 100% concordance with the freshly amplified SCM samples. Then, SCM and trophectoderm (TE) samples from 149 blastocysts from 51 couples were collected. A 98.0% successful SCM sample amplification rate (146/149) was achieved. For the 146 paired TE biopsy and SCM samples, the overall concordance rate was 82.9% (121/146). Ten embryos with aneuploid TE results but euploid niPGT results were donated. A 70.0% (7/10) true negative rate was achieved by niPGT with respect to the inner cell mass (ICM) results (TE-positive embryos). CONCLUSIONS: These results suggested that SCM stored at -80 °C for 6 months without affecting niPGT results based on NICSInst amplification.

Humans↗

PubMed1986

Maternal administration of cyclophosphamide induces chromosomal aberrations and inhibits cell number, histone synthesis, and DNA synthesis in preimplantation mouse embryos.

The effects of cyclophosphamide (CPA), administered to pregnant inbred CBA/Ca mice 60 h after copulation, on cell number, mitotic index, chromosome structure, histone synthesis, and DNA synthesis of 84-h blastocysts, and the subsequent development of these blastocysts cultured for a further 120 h in vitro are described. Cyclophosphamide 4, 20, and 40 mg/kg significantly increased the number of chromosomally aberrant cells, chromosomal aberrations, and chromosome breaks in the blastocysts. Chromosomal rearrangements were significantly increased in the CPA 20 and 40-mg/kg treated groups, and in the 40-mg/kg group the number of cells with ring chromosomes was significantly increased. Histone synthesis and DNA synthesis were significantly inhibited in the CPA 20 and 40-mg/kg treated groups. Blastocyst cell number in each of the treated groups was less than the controls. On subsequent culture in vitro, significantly fewer embryos in the CPA 20 and 40-mg/kg groups hatched, attached, developed trophoblast outgrowths, and expanded their inner cell masses. However, the differentiation of inner cell mass into ectoderm and endoderm was impaired by all three doses of the drug. These results demonstrate that CPA administered to pregnant mice 60 h after copulation has a clastogenic effect and interferes with synthesis of DNA and histones in the preimplantation embryo, and that the drug inhibits the subsequent development and differentiation of these embryos. Cytogenetic analysis of preimplantation embryos might be a useful adjunct to the existing methods in the evaluation of the embryotoxicity of drugs and chemicals.

Animals↗

PubMed1985

Fibronectin visualized by scanning electron microscopy immunocytochemistry on the substratum for cell migration in Xenopus laevis gastrulae.

In amphibian gastrulae, scanning electron microscopy (SEM) has shown the presence of a network of extracellular fibrils on the inner aspect of the ectoderm layer, which serves as the substratum for migration by the presumptive mesoderm cells. In vitro experiments have shown that the fibril network promotes attachment and migration by mesoderm cells, and probably guides the migration by contact guidance. Filopodia of the migrating cells showed preferential attachment to the fibrils. Use of a colloidal gold probe for SEM immunocytochemistry has shown that fibrils observed by SEM contain fibronectin, probably as a major component. This provides direct evidence that the extracellular matrix containing fibronectin provides the substratum and guides cell migration in morphogenetic movement.

Animals↗

PubMed1984

Extracellular matrix and neural determination during amphibian gastrulation.

Previous studies have shown the presence of a network of extracellular matrix on the inner surface of the ectoderm of the early gastrulae Pleurodeles waltlii. Similar dense networks have been described by other authors in another Urodele species and in Anurans. It now seems well established that this extracellular material (ECM) has important functions in the mechanisms of morphogenetic cell movements during gastrulation. The results reported here provide evidence that this ECM is not implicated in the transmission of the neuralizing signal at the gastrula stage, and therefore is not involved in the process of neural determination.

Animals↗

PubMed1998

Mouse embryonic stem cells with aberrant transforming growth factor beta signalling exhibit impaired differentiation in vitro and in vivo.

Embryonic stem (ES) cells are resistant to transforming growth factor beta (TGF beta). We have shown previously that they lack type-II binding receptors (T beta RII) and in this respect resemble the inner cell mass and ectoderm cells of mouse embryos 4.5-7.5 days post coitum (dpc); they do however express type-I (alk-5) signalling receptors. Here we show that in contrast to several tumour cell lines, stable transfection of wtT beta RII is not sufficient for ES cells to become biologically sensitive to TGF beta. We analysed the expression of several down-stream molecules known to be involved in TGF beta signalling (Smads) and TGF beta-mediated cell cycle regulation (cyclins D) during the differentiation of control and wtT beta RII-expressing ES cells and showed that upregulation of these molecules correlated with (i) an increase in plasminogen activator inhibitor-1 (PAI-1) synthesis and (ii) growth inhibition, following addition of TGF beta 1. These TGF beta responses were reduced in an ES cell line expressing a dominant negative (truncated) T beta RII (delta T beta RII). The differentiation pattern of control and wtT beta RII-expressing ES cells was indistinguishable in monolayer culture and as embryoid bodies, but in delta T beta RII ES cells, the capacity to form mesodermal derivatives in monolayer cultures in response to the addition of retinoic acid (RA) and removal of leukemia inhibitory factor (LIF) was lost, and only endoderm-like cells formed. The T beta RII and delta T beta RII ES cells were, however, both distinguishable from control ES cells when allowed to differentiate in chimaeric embryos following aggregation with morula-stage hosts. Conceptuses containing mutant cells, recovered from pseudopregnant females at the equivalent of 9.5 dpc, exhibited highly defective yolk sac development; most strikingly, no blood vessels were present and in addition the yolk sacs with derivatives of ES cells containing wtT beta RII were blistered and lacked haematopoietic cells. The implications for understanding TGF beta signalling in early mouse development are discussed.

Animals↗

PubMed1982

Movement and guidance of migrating mesodermal cells in Ambystoma maculatum gastrulae.

A scanning electron microscopic study in early gastrulae of Ambystoma maculatum showed that migrating presumptive mesodermal cells were strongly oriented toward the animal pole. They had lamellipodia and filopodia at their leading edges, and rounded or tapering, tail-like, trailing edges. Of the cells whose polarization could be determined unequivocally, 81% appeared to be directed in a quadrant toward the animal pole, and 93% were directed to some extent away from the blastopore. This strong orientation suggests that specific mechanisms direct cell movement, in addition to the non-specific dispersive mechanism of the contact inhibition of cell movement. There is a network of fine extracellular fibrils that covers the inner surface of the ectodermal layer. Filopodia of the migrating cells frequently attach to and appear to follow the fibrils, suggesting that the fibrils serve as a guiding substratum for cell attachment and movement. There are areas where the fibrils are apparently aligned along the blastopore-animal pole axis, and a preliminary statistical analysis using micrographs at high magnification showed a significant alignment parallel to the blastopore-animal pole axis. This fibril alignment could cause the strong orientation of the mesodermal cells by means of contact guidance.

Ambystoma↗

PubMed1986

Presumptive mesoderm cells from Xenopus laevis gastrulae attach to and migrate on substrata coated with fibronectin or laminin.

During amphibian gastrulation, presumptive mesoderm cells migrate from the blastopore towards the animal pole along the inner surface of the ectodermal layer. Their natural substratum is a network of anastomosing extracellular matrix fibrils, which contains fibronectin and laminin, as shown by immunostaining. If the fibril network is transferred onto a coverslip from the ectodermal layer, dissociated mesodermal cells readily attach to such conditioned surfaces and show active migration in a medium of high pH and low calcium ion concentration. In the present study, the surface of tissue culture dishes was coated with fibronectin, laminin, collagen type IV or heparan sulphate, to examine the effects on cell attachment and movement. The presumptive mesoderm cells from Xenopus laevis gastrulae showed rapid adhesion and active movement on the fibronectin- or laminin-coated surfaces. Cell adhesion was stronger and the mean rate of movement was higher on the fibronectin-coated surface than on the laminin-coated surface. The dissociated ectodermal cells did not attach to the fibronectin- or laminin-coated surfaces. The mesodermal cells did not attach to the collagen-, or heparan sulphate-coated surfaces, showing that these components of the basement membrane cannot serve as an adequate substratum for the mesoderm cells, at least by themselves.

Animals↗

PubMed2000

Expression of N-CAM-180 and N-cadherin during development in two South-American anuran species (Bufo arenarum and Hyla nana).

Cadherins and N-CAM are Ca++-dependent and Ca++-independent cell adhesion molecules respectively. These molecules play a key role in morphogenesis and histogenesis. We determined the spatiotemporal pattern of N-cadherin and N-CAM-180 kDa expression by immunohistochemistry during development in two South-American anuran species (Bufo arenarum, toad and Hyla nana, frog). Both N-cadherin and N-CAM were not detectable during early developmental stages. Expression of N-cadherin appeared between the inner and the outer ectoderm layers at stages 19-20. At stages 24-25, N-cadherin was expressed in the neural tube and the heart. In early tadpoles, N-cadherin expression increased along with the central nervous system (CNS) morphogenesis, and reached its maximum level at metamorphic climax stage. N-Cadherin expression was not uniformly distributed. At stage 42, olfactory placodes and retina expressed N-cadherin. Contrary to N-CAM, the strongly myelinated cranial nerves were not labeled. N-Cadherin was present in several mesoderm derivatives such as the notochord, heart and skeletal muscle. The non-neural ectoderm and the endoderm were always negative. Expression of N-CAM appeared first in the neural tube at stages 24-25 and the level of expression became uniform from pre-metamorphic to metamorphic climax tadpoles. At this latter stage, a clear N-CAM immunolabeling appeared in the nerve terminals of pharynx and heart. N-Cadherin and N-CAM were found mainly co-expressed in the CNS from early tadpole to metamorphic climax tadpole. Our results show that the expression of N-CAM and N-cadherin is evolutionary conserved. Their increased expression during late developmental stages suggests that N-CAM and N-cadherin are involved in cell contact stabilization during tissue formation.

Animals↗

PubMed1979

Scanning electron microscopy (SEM) of cranial neural crest migration in chick embryos.

This study describes migrating cranial neural crest cells and the microenvironment through which they migrate in chick embryos. Just prior to and during cell migration, an extensive fibrillar meshwork is observed, particularly on the outer surface of the neural tube and the inner surface of the ectoderm. This meshwork in general had a random orientation. This suggested to us that the meshwork does not provide a directive vector for cell migration but rather a substratum to promote or enhance crest cell filopodial attachment as the cells migrate. Much remains to be done in characterizing the composition of this meshwork. Based on other studies in which a smiliar meshwork has been observed, it is not unreasonable to consider it to be partly collagenous. Another major component in the relatively cell-free space through which avian crest cells migrate is hyaluronic acid. The migrating crest cells are characteristically bipolar and are generally oriented in the direction of migration, although little is known about the actual mechanism of motility. Alterations in the migrating cell or in the environment through which it migrates may interfere with normal craniofacial morphogenesis, as discussed elsewhere in this volume by Johnston and Sulik.

Animals↗

PubMed1980

In vitro development of inner cell masses isolated from t0/t0 and tW5/tW5 mouse embryos.

Inner cell masses (ICMs) isolated immunosurgically from mouse blastocysts segregating the homozygous lethal mutants t0/t0 and tW5/tW5 were cultured in vitro. Presumed t0/t0 ICMs fail to grow after three days in culture (equivalent gestational day 7.5) when they consist of an outer layer of endoderm cells surrounding about 30 epiblast cells. Presumed homozygous tW5/tW5 ICMs develop to a more advanced stage in culture and on the seventh day (equivalent gestational day 11.5) consist of an inner core of disorganized ectoderm cells with a small proamniotic cavity, surrounded by multiple layers of endoderm cells.

Animals↗

PubMed1998

Cloning of the Xenopus integrin alpha(v) subunit and analysis of its distribution during early development.

One striking feature of the integrin alpha(v) subunit is its ability to associate with at least five different beta subunits (beta1, beta3, beta5, beta6 and beta8) to form functional receptors. These receptors are involved in diverse biological processes, such as differentiation, cell adhesion and migration. Here we report the cloning of the Xenopus homolog of the integrin alpha(v) subunit. Integrin alpha(v) mRNA and protein are maternally supplied and present throughout development. During gastrulation and neurulation alpha(v) protein appears on cell membranes of all three germ layers. In tailbud stage embryos great amounts of the alpha(v) protein can be observed in the inner layer of the ectoderm and in the endothelial cells lining the pharynx and gut.

Amino Acid Sequence↗

PubMedDate not supplied

Keratitis, ichthyosis, and deafness (KID syndrome): review of the literature and proposal of a new terminology.

The so-called KID (keratitis, ichthyosis, deafness) syndrome is a congenital disorder of ectoderm that affects not only the epidermis, but also other ectodermal tissues such as the corneal epithelium and the inner ear. Sixty-one patients who fulfill the criteria for this syndrome were identified in a review of the literature through December 1993. All had cutaneous and auditory abnormalities, and 95% also had ophthalmologic defects. The most frequent clinical features were neurosensory deafness 90%, erythrokeratoderma 89%, vascularizing keratitis 79%, alopecia 79%, and reticulated hyperkeratosis of the palms and soles 41%. All of these findings constitute the major criteria for the diagnosis. The KID acronym does not accurately define this entity since the disorder is not an ichthyosis, because scaling is not the main cutaneous feature and not all patients have keratitis early in the course. We suggest that this syndrome should be included under the general heading of congenital ectodermal defects as a keratodermatous ectodermal dysplasia (KED).

Adult↗

PubMed1996

Positive and negative signals modulate formation of the Xenopus cement gland.

The cement gland is a simple secretory organ that marks the anterior-most dorsal ectoderm in Xenopus embryos. In this study, we examine the timing of cement gland induction and the cell interactions that contribute to cement gland formation. Firstly, we show that the outer ectodermal layer, from which the cement gland arises, becomes specified as cement gland by mid-gastrula. Curiously, at early gastrula, the inner layer of the dorsal ectoderm, which does not contribute to the mature cement gland, is strongly and transiently specified as cement gland. Secondly, we show that the mid-gastrula dorsoanterior yolky endoderm, which comes to underlie the cement gland primordium, is a potent inducer of cement gland formation and patterning. The cement gland itself has an anteroposterior pattern, with the gene XA expressed only posteriorly. Dorsoanterior yolky endoderm greatly enhances formation of large, patterned cement glands in partially induced anterodorsal ectoderm, but is unable to induce cement gland in naive animal caps. Neural tissue is induced less frequently than cement gland by the dorsoanterior yolky endoderm, suggesting that the endoderm induces cement gland directly. Thirdly, we demonstrate that the ventral ectoderm adjacent to the cement gland attenuates cement gland differentiation late during gastrulation. The more distant ventral mesendoderm is also a potent inhibitor of cement gland formation. These are the first data showing that normal ventral tissues can inhibit cement gland differentiation and suggest that cement gland size and position may be partly regulated by negative signals. Previous work has shown that cement gland can be induced by neural plate and by dorsal mesoderm. Together, these data suggest that cement gland induction is a complex process regulated by multiple positive and negative cell interactions.

Animals↗

PubMed2003

A restrictive role for Hedgehog signalling during otic specification in Xenopus.

Vertebrate inner ear development is initiated by the specification of the otic placode, an ectodermal structure induced by signals from neighboring tissue. Although several signaling molecules have been identified as candidate otic inducers, many details of the process of inner ear induction remain elusive. Here, we report that otic induction is responsive to the level of Hedgehog (Hh) signaling activity in Xenopus, making use of both gain- and loss-of-function approaches. Ectopic activation of Hedgehog signaling resulted in the development of ectopic vesicular structures expressing the otic marker genes XPax-2, Xdll-3, and Xwnt-3A, thus revealing otic identity. Induction of ectopic otic vesicles was also achieved by misexpression of two different inhibitors of Hh signaling: the putative Hh antagonist mHIP and XPtc1deltaLoop2, a dominant-negative form of the Hh receptor Patched. In addition, misexpression of XPtc1deltaLoop2 as well as treatment of Xenopus embryos with the specific Hh signaling antagonist cyclopamine resulted in the formation of enlarged otic vesicles. In summary, our observations suggest that a defined level of Hh signaling provides a restrictive environment for otic fate in Xenopus embryos.

Animals↗

PubMed2000

Induction of inner ear fate by FGF3.

Loss-of-function experiments in avians and mammals have provided conflicting results on the capacity of fibroblast growth factor 3 (FGF3) to act as a secreted growth factor responsible for induction and morphogenesis of the vertebrate inner ear. Using a novel technique for gene transfer into chicken embryos, we have readdressed the role of FGF3 during inner ear development in avians. We find that ectopic expression of FGF3 results in the formation of ectopic placodes which express otic marker genes. The ectopically induced placodes form vesicles which show the characteristic gene expression pattern of a developing inner ear. Ectopic expression of FGF3 also influences the formation of the normal orthotopic inner ear, whereas another member of the FGF family, FGF2, shows no effects on inner ear induction. These results demonstrate that a single gene can induce inner ear fate and reveal an unexpectedly widespread competence of the surface ectoderm to form sensory placodes in higher vertebrates.

Animals↗

PubMed2003

Expression of mouse fibroblast growth factor and fibroblast growth factor receptor genes during early inner ear development.

The inner ear, which mediates hearing and equilibrium, develops from an ectodermal placode located adjacent to the developing hindbrain. Induction of the placode and its subsequent morphogenesis and differentiation into the inner ear epithelium and its sensory neurons, involves signalling interactions within and between otic and non-otic tissues. Several members of the fibroblast growth factor (FGF) family play important roles at various stages of otic development; however, there are additional family members that have not been evaluated. In this study, we surveyed the expression patterns of 18 mouse Fgf and 3 Fgf receptor (Fgfr) genes during early otic development. Two members of the Fgf family, Fgf4 and Fgf16, and all three tested members of the Fgfr family, Fgfr2c, Fgfr3c, and Fgfr4, were expressed in tissues relevant to inner ear development. Fgf4 transcripts were expressed in the preplacodal and placodal ectoderm, suggesting potential roles in placode induction and/or maintenance. Fgf16 was expressed in the posterior otic cup and vesicle, suggesting roles in otic cell fate decisions and/or axis formation.

Animals↗